Mechanisms of ERK phosphorylation triggered via mouse formyl peptide receptor 2

Filina, Julia; Tikhonova, Irina V.; Gabdoulkhakova, Aida; Rizvanov, Albert A.; Safronova, V. G.

doi:10.1016/j.bbamcr.2022.119356

Cited by 5 publications

(2 citation statements)

References 80 publications

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“…Among the cytosolic proteins, p47 PHOX is an adaptor subunit essential for the assemble of NADPH oxidase [ 37 ]. Previous studies suggested that p47 PHOX could translocate to the membrane after phosphorylation by ERK1/2 and AKT [ 38 , 39 ]. In LPS-primed neutrophils, 6-OAU stimulation could induce the translocation of p47 PHOX to the plasma membrane, while this effect could not be observed in GPR84 –/– neutrophils (Fig.…”

Section: Resultsmentioning

confidence: 99%

GPR84 regulates pulmonary inflammation by modulating neutrophil functions

Wang

Zhang

et al. 2023

Acta Pharmacol Sin

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Acute lung injury (ALI) is an acute, progressive hypoxic respiratory failure that could develop into acute respiratory distress syndrome (ARDS) with very high mortality rate. ALI is believed to be caused by uncontrolled inflammation, and multiple types of immune cells, especially neutrophils, are critically involved in the development of ALI. The treatment for ALI/ARDS is very limited, a better understanding of the pathogenesis and new therapies are urgently needed. Here we discover that GPR84, a medium chain fatty acid receptor, plays critical roles in ALI development by regulating neutrophil functions. GPR84 is highly upregulated in the cells isolated from the bronchoalveolar lavage fluid of LPS-induced ALI mice. GPR84 deficiency or blockage significantly ameliorated ALI mice lung inflammation by reducing neutrophils infiltration and oxidative stress. Further studies reveal that activation of GPR84 strongly induced reactive oxygen species production from neutrophils by stimulating Lyn, AKT and ERK1/2 activation and the assembly of the NADPH oxidase. These results reveal an important role of GPR84 in neutrophil functions and lung inflammation and strongly suggest that GPR84 is a potential drug target for ALI.

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Section: Resultsmentioning

confidence: 99%

GPR84 regulates pulmonary inflammation by modulating neutrophil functions

Wang

Zhang

et al. 2023

Acta Pharmacol Sin

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“…They reveal a concerted action between GPCR kinase 2 (GRK2),  arrestins and the actin cytoskeleton. Filina et al examined the impact of activation of formyl peptide receptors in granulocytes and how this leads to ERK phosphorylation [8]. The authors revealed an important and proximal role for early ROS generation through NADPH oxidase to boost ERK activation and activity by enhancing MEK (a kinase phosphorylating ERK) activity as well as inhibiting Dual Specificity Protein Phosphatase 6 (a phosphatase dephosphorylating ERK).…”

Section: Signaling From Surface Receptorsmentioning

confidence: 99%